The enzyme carnitine acyltransferase 1 (CAT-1) resides on the inner face of the outer mitochondrial membrane and is responsible for converting acyl-CoA into carnitine esters for the purpose of transporting acyl groups into the mitochondria for beta-oxidation. During ischemia or hypoxia, beta-oxidation is inhibited by the high mitochondrial redox potential, which results in a build-up of long-chain acylcarnitines (LCA) in the cytosol. LCA, in turn, has been shown to mediate a number of deleterious events in ischemic tissue. These include activation of calcium channels, increase in cytosolic calcium and electrophysiological derangements resulting from their incorporation into the sarcolemma of the cardiac myocyte. Thus CAT-I inhibitors can prevent injury to ischemic tissue, i.e., can limit infarct size, improve cardiac function and prevent arrhythmias during and following a myocardial infarction.